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What are chemical candidates for replicator molecule?

What are chemical candidates for replicator molecule?


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I have readSelfish geneby Richard Dawkins and idea is that at random some molecule was synthesized that had a property if there is enough 'materials' to construct copy of itself - it would. And then it made bunch of it's copies and then copies started mutating and eventually we got to DNA in us.

In his book he never says what actual molecule is original replicator.

What are chemical candidates for original replicator molecule?


There is no accurate answer , as you say we talk about candidates . there is lots of strong theories about the origin of self replicators . RNA world was a strong candidate since latest experiments that suggest there is a good chance that some molecules that have simpler structure than RNA , could have a chance to do self replications . there is also strong theories such as :

1.Prions that delivered by space objectives and Meteorites .

2.Life's origins may result from low-energy electron reactions in space:

http://phys.org/news/2016-06-life-result-low-energy-electron-reactions.html


first self-replicator recreated in lab:

RNA, or something very like it, has long been a strong candidate as the first self-replicating molecule in the origin of life. This is because it can both catalyse chemical reactions and carry genetic information. But chemists first needed to explain how a large, complex molecule like RNA could form spontaneously to begin the process. They had done so for some, but not all, components of the RNA molecule.

https://www.newscientist.com/article/2088006-building-blocks-of-lifes-first-self-replicator-recreated-in-lab/

The origin of replicators and reproducers:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664675/

you can also check the topic :The RNA World and the Origins of Life from the book :

Molecular biology of the cell by Alberts B, Johnson A, Lewis J, et al.


after all this article was so innovative for me . I think it's a good explanation for self replication of molecules simpler than RNA.

http://www.nanowerk.com/nanotechnology-news/newsid=40896.php

"Maslov and Tkachenko's model imagines some kind of regular cycle in which conditions change in a predictable fashion-say, the transition between night and day. Imagine a world in which complex polymers break apart during the day, then repair themselves at night. The presence of a template strand means that the polymer reassembles itself precisely as it was the night before. That self-replication process means the polymer can transmit information about itself from one generation to the next. That ability to pass information along is a fundamental property of life"


What are chemical candidates for replicator molecule? - Biology

The first ancestor to all life was a self-replicating entity capable of evolving but must have been much simpler than a cell that is, a molecular replicator.

Recent work on RNA polymerase ribozymes supports the view that the molecular replicator was made of RNA, and no other molecule was required (the RNA World).

The RNA World is challenged by the fact that a self-replicating RNA polymerase ribozyme has yet to be demonstrated and that little evidence for its existence is seen in life today as well as problems in how the transition from RNA-only to RNA–protein world could have occurred.

A molecular replicator with two components –RNA and peptide – overcomes these problems and may be a better fit.

Evolution requires self-replication. But, what was the very first self-replicator directly ancestral to all life? The currently favoured RNA World theory assigns this role to RNA alone but suffers from a number of seemingly intractable problems. Instead, we suggest that the self-replicator consisted of both peptides and nucleic acid strands. Such a nucleopeptide replicator is more feasible both in the light of the replication machinery currently found in cells and the complexity of the evolutionary path required to reach them. Recent theoretical and mathematical work supports this idea and provide a blueprint for future investigations.


Rotaxane raises the bar for self-replicating chemical systems

Scientists in the UK and Malaysia have created a self-assembling rotaxane that can replicate itself. The result may lead to the development of autonomous chemical systems that mimic cellular processes.

American Chemical Society

During self-replication, a 1,3-dipolar cycloaddition forms a new rotaxane thread

Life is adept at faithfully reproducing complex molecules such as DNA and many research groups are attempting to re-create similar phenomena in the lab using a library of synthetic chemicals. ‘Self-replication processes are inherently interesting from the point of view of biology as the self-replication of molecules (ie DNA) is the chemical basis of life,’ remarks Steve Goldup, an organic synthesis researcher from the University of Southampton, UK, who was not involved in the work.

But copying the way in which such complex molecules self-replicate using just lab chemicals has proven to be very difficult. ‘We’ve published a body of work … where we’ve made small molecules that are capable of copying themselves,’ comments Douglas Philp from the University of St Andrews. ‘Just having a small molecule that replicates itself is not … ultimately very complex.’

Philp and his colleagues wanted to create an intricate synthetic replicator to demonstrate that it may one day be possible to construct a chemical network that could behave like a protocell – a simple self-replicating body that could be a stepping-stone towards life. For the group, the ideal candidate for this was a rotaxane – a dumbbell-shaped compound that is threaded through a cyclic molecule.

Philp explains that the initial synthesis of a rotaxane is ‘quite conventional’. Often, a thread molecule is held within a macrocycle before this pseudorotaxane is capped at each end via a simple functionalisation reaction. But in this scenario both ends are inert and cannot facilitate replication.

American Chemical Society

The rotaxane stopper's imide group initiates the self-replication process

The solution was to ensure one of the ends acts as a reactive site. ‘So effectively you have a rotaxane that has a linear component with two stoppers,’ says Philp. ‘One of the stoppers is inert … and the other stopper is actually replicating.’ Under these conditions, Philp and his colleagues were able to produce a pseudorotaxane with a macrocyclic amide threaded onto it. The reactive cap is a nitrone, which also acts as the initiator for replication and, with the help of two recognition molecules, amidopyridine and carboxylic acid, the rotaxane can be copied from the existing pseudorotaxane scaffold. The building blocks for these scaffolds were synthesised in a number of different solutions, with the thread and rotaxane both being constructed in deuterated chloroform.

Although the rotaxane is able to self-replicate, there have been some issues in how much rotaxane can ultimately be generated. Philp explains that the macrocycle may react with the nitrone and block any further replication: ‘If it does that, then effectively the system is dead because the nitrone is the reactive bit and can’t react.’

The fact that Philp’s team have created a self-replicating rotaxane system in the first place, irrespective of its inefficiencies, is a promising sign, according to Goldup. ‘The example here pushes the boundaries of what has been demonstrated up until now in artificial reaction systems,’ Goldup tells Chemistry World. ‘Implementing self-replication into these systems brings the idea of an autonomous chemical nanotechnology a (very small) step closer.’


Community metabolism

The common ancestor of the now existing cellular lineages (eukaryotes, bacteria, and archaea) may well have been a community of organisms that readily exchanged components and genes. It would have contained:

  • Autotrophs that produced organic compounds from CO2 either photosynthetically or by inorganic chemical reactions
  • Heterotrophs that obtained organics by leakage from other organisms
  • Saprotrophs that absorbed nutrients from decaying organisms
  • Phagotrophs that were sufficiently complex to envelop and digest particulate nutrients including other organisms.

The eukaryotic cell seems to have evolved from a symbiotic community of prokaryotic cells. It appears that DNA-bearing organelles like mitochondria and chloroplasts are remnants of ancient symbiotic oxygen-breathing bacteria and cyanobacteria, respectively, where at least part of the rest of the cell may have been derived from an ancestral archaean prokaryote cell. This concept is often termed the endosymbiotic theory but is perhaps better considered as an hypothesis. There is still debate about whether organelles like the hydrogenosome predated the origin of mitochondria, or vice versa: see the hydrogen hypothesis for the origin of eukaryotic cells.

How the current lineages of microbes evolved from this postulated community is currently unsolved but subject to intense research by biologists, stimulated by the great flow of new discoveries emerging from genome science. [4]


Results

We have performed a systematic simulation study to reveal the effects of changing the model parameters critical for the coexistence of the replicators. Since the mean-field approximation (i.e., the well-mixed version) of the MRM system is not coexistent (c.f. [24]) the spatial aspects of the present model are of crucial interest from the viewpoint of system persistence and stability. We focused our interest on three parameters which are separated into two groups: those related to 1) the mobility of replicators (the size of the replication neighbourhood (r), and mobility of replicators on the surface, D) and 2) to metabolite/monomer diffusibility on the surface (the size of metabolic neighbourhoods, h). Other parameters were kept constant throughout the simulations. Lattice size was L =�󗌀 simulations were initiated with n =𠂔 replicator types randomly assigned to 80% of the sites at t =𠂐. The decay rate was d =𠂐.2, the claim of empty sites for remaining empty was Ce =𠂒.0, and the replication rates of the four different replicator types were k1 =𠂓.0, k2 =𠂕.0, k3 =𠂗.0 and k4 =𠂙.0. In simulations with parasitic replicators present the parasite was the fourth type added to the community of three metabolically cooperating replicators the replication rate of the parasite was kp =𠂙.0.

The model was coded in C, compiled with gcc (GNU C Compiler 4.4.5) and run under Linux (Debian 6.0.1). For each parameter set we have produced 5 replicate runs with different random number sequences. The conclusions of a long series of batch simulations are the following:

The effects of local monomer production/consumption and limited replicator diffusion

Figure  2 shows simulation results of the MRM at different sizes of the replication neighbourhood (r) and the metabolic neighbourhood (h), with different values of the replicator diffusion parameter (D) at a fixed system size (n =𠂔). The main effects showing up on Figure  2 are:

Coexistence of metabolic replicators as the function of replicator diffusion (D), metabolic (h) and replication (r) neighbourhood size. The panels of the figure differ in the number of diffusion steps per generation: Panel A: D =𠂐, Panel B: D =𠂑, Panel C: D =𠂔 and Panel D: D =�. x- and y-axes are the sizes of metabolic neighbourhoods (h) and replication neighbourhoods (r) respectively (N: von Neumann neighbourhood 3: 3൳, 5: 5൵, 7: 7൷, 25: 25휥 and 37: 37휷 Moore neighbourhoods). The grayscale shades correspond to average replicator densities (%) on the whole grid at the end of the simulations (i.e., for t =𠂑.000). The numbers within panels indicate coexistent/extinct replicate simulations out of the five repetitions with the same parameter set and different pseudo-random number sequences.

a) system persistence and total replicator population densities depend on all three space-related model parameters (r, h and D)

b) increasing replication neighbourhood size (r) or replicator diffusion (D) or both are advantageous for persistence and population density

c) persistence and population density follow optimum courses with the size of the metabolic neighbourhood (h): too small and too large h are both fatal for the system

d) persistent systems attain high population densities

e) the results are robust with respect to persistence: 5 replicate runs almost always (with only a single exception) produce the same outcome (with low standard deviations): either always persistence or always extinction, depending on the actual parameter set. Note that the replicator populations reach their equilibrium densities during the simulations of 1.000 generations each.

The effect of spatial parameters on the maximum attainable system size

We have tested the MRM system for the maximum number of metabolic replicator types (i.e., the largest system size nmax= q) that can coexist at different parameter sets. The results are condensed into Figure  3 , with the following conclusions:

The maximum number of coexisting metabolic replicators as the function of replicator diffusion (D), metabolic (h) and replication (r) neighbourhood size. The panels of the figure differ in the number of diffusion steps per generation: Panel A: D =𠂐 , Panel B: D =𠂑, Panel C: D =𠂔 and Panel D: D =� x- and y-axes are the sizes of metabolic neighbourhoods (h) and replication neighbourhoods (r) respectively (N: von Neumann neighbourhood 3: 3൳, 5: 5൵, 7: 7൷, 25: 25휥 and 37: 37휷 Moore neighbourhoods). The numbers within panels show the maximum number of coexisting metabolic replicator types (nmax= q) for the given parameter set. Other parameters: pd =𠂐.2, Ce =𠂒.0, ki =𠂓.0 +𠂒.0i (i =𠂐, . max). (max. is the maximal number of replicators that can be seen within a square on the panel).

f) q follows a course with increasing r, h and D similar to that of system persistence and total population density at n =𠂔: increasing r and D are beneficial, too low and too high h are adverse for the maximum number of coexistent replicators

g) within the parameter range tested the largest system size can go up to about nmax =� different replicator types under optimal conditions.

The effect of parasites

Figure  4 shows the results of a series of simulations with all the parameters set to exactly the same values as in the simulations that produced Figure  2 , except that the 4th replicator is a parasitic one: it does not contribute to metabolism at all, but uses the product of metabolism – i.e., monomers – for its own replication (Figure  1 B). The parasite is the fastest of the four types in replication, with kp =𠂙.0 (compared to k1 =𠂓.0, k2 =𠂕.0 and k3 =𠂗.0 of the cooperating types). Figure  4 suggests the following conclusions:

Coexistence of metabolic replicators and a parasitic one as the function of replicator diffusion (D), metabolic (h) and replication (r) neighbourhood size. The panels of the figure differ in the number of diffusion steps per generation: Panel A: D =𠂐, Panel B: D =𠂑, Panel C: D =𠂔 and Panel D: D =�. x- and y-axes are the sizes of metabolic neighbourhoods (h) and replication neighbourhoods (r) respectively (N: von Neumann neighbourhood 3: 3൳, 5: 5൵, 7: 7൷, 25: 25휥 and 37: 37휷 Moore neighbourhoods). The grayscale shades correspond to average replicator densities (%) on the whole grid at the end of the simulations (i.e., for t =𠂑.000). The numbers within panels indicate coexistent/extinct replicate simulations out of the five repetitions with the same parameter set and different pseudo-random number sequences. The third number is the number of replicate simulations in which the parasite died out.

h) replacing a metabolic cooperator with a parasite does not do much harm to the metabolic system as a whole: the parameter range of coexistence does not shrink. (In fact it expands in this case, but this is due to the simultaneous decrease of system size from n =𠂔 to n =𠂓 – see the Discussion for an explanation)

i) at very small metabolic neighbourhood sizes the parasite may be expunged from the metabolic system completely

j) increasing the mobility of the replicators (i.e., larger values of D and/or r) favours the parasite in terms of its chances of survival and equilibrium abundance, but even at high replicator mobility the parasite is unable to exclude metabolic cooperators and to ruin the metabolic system

k) the parasitized metabolic system is also robust with respect to persistence: only a few borderline cases deviate from unequivocal coexistence or unequivocal extinction in 5 replicate simulations.


Peering into the cellular cycle

The development of chemical tools and small-molecule inhibitors enables the resolution of critical cellular processes with high spatial and temporal precision.

Cells, like all living entities, are born, interact with the surrounding environment and eventually die. The field of cell biology has historical roots in the field of microscopy, enabling visualization of these processes with high resolution. However, approaches to alter cell division, cellular interactions and death, often by genetic and biochemical means, have lagged in their ability to enable spatial and temporal disruption with precision. Chemical biology is well suited to develop improved tools that enable the manipulation of cellular processes with the desired resolution. In this themed issue, we offer a collection of pieces focusing on this intersection of chemical approaches with cell biology and highlighting how this interface may reveal new insights.

Eukaryotic cells are born from a single parental cell through a series of temporally defined phases called mitosis. In particular, the parental cell undergoes a division process producing two daughter cells, each inheriting a single set of chromosomes. Each mitotic phase is regulated by a dynamic and complex set of protein assemblies, and cell biology and chemical tools have been essential in defining the molecular and regulatory basis of these complexes. Given that many cell division events occur at the second or minute time scale, small molecules offer advantages over genetic perturbations in terms of reversibility and temporal control. Early studies utilized general mitotic inhibitors such as colchicine and taxol, which disrupted spindle function and arrested cells at particular mitotic stages. However, these reagents lacked a defined molecular target, limiting their ability to probe the function of an individual mitotic component.

Chen and Lampson discuss recent advances using small molecules to inhibit specific cell cycle regulators that reveal complex interactions not observed with other types of perturbations. One example is apcin, which targets the APC/C E3 ubiquitin ligase complex, which normally promotes mitotic exit. A study of apcin revealed opposing effects through a different regulatory context such as high activity of the spindle assembly checkpoint. In addition, Chen and Lampson describe the development of chemical tools such as optogenetic chemical dimerizers that can direct cell cycle regulators to particular chromosome regions with blue-light exposure. Recent work using these dimerizers to direct the CENP-E kinetochore motor to chromosomes supported a role of CENP-E as a critical motor directing chromosomes to the spindle equator.

During its lifetime, a cell interacts with its environmental surroundings, especially with neighboring cells. Precise cell-to-cell communication is required for many physiological processes such as tissue formation, and this entails complex and transient interactions between cell surface molecules. An earlier Commentary proposed the need for chemical tools to detect, disrupt and reconstitute these intracellular networks. Since that time, advances in microscopy, chemical tagging and cell engineering approaches have enabled progress in this area, summarized in a Review by Bechtel et al. Chemical biology approaches have enabled essential advances for example, a proximity biotinylation strategy to identify unique peptides secreted by particular cell types, a light-inducible spatial proximity system that modifies proteins on neighboring cells and the use of unnatural amino acid technology to construct a switch for chimeric antigen receptor T cells that interact with cell surface tumor-specific antigens.

In response to detrimental cellular or environmental conditions, a cell can undergo various forms of death, ranging from apoptosis to ferroptosis, each of which is defined by unique morphological features and molecular markers. Ferroptosis is a non-apoptotic type of cell death that is distinguished by the accumulation of iron-dependent membrane lipid hydroperoxides, resulting in membrane rupture. Given the heavy lipid dependence and involvement of hydroxyl radicals, the study of ferroptosis has been served well by chemical biology approaches. CRISPR-genome screens and lipidomics have identified critical mediators of ferroptosis such as cytochrome P450 oxidoreductase and phosphatidylethanolamines. Mass spectrometry approaches have enabled detection of oxidized phosphatidylethanolamines in ferroptotic cardiomyocytes with improved resolution, while high-throughput small-molecule profiling studies have revealed candidates for chemical modulation. In particular, the use of a high-throughput time-lapse cell death imaging assay enabled profiling of compounds such as rapamycin and PI3K inhibitors that alter ferroptosis directly or indirectly.

Another form of cell death is necroptosis, which is responsive to apoptotic stimuli but does not involve apoptotic regulators such as caspases. Like studies on ferroptosis, chemical biology has helped guide new mechanistic insights and tools for altering necroptosis. One of the first papers published in our journal defined the necroptosis pathway by identification of an inhibitor called necrostatin-1, which targeted the critical regulator RIPK3. RIPK3 recruits the pseudokinase mixed lineage kinase domain-like (MLKL) to necrosomes. The recent generation of monobodies, which are synthetic binding proteins, against specific conformations of MLKL revealed that a conformational transition is needed for MLKL activation.

Damaged cellular organelles and proteins need to be disposed of properly to maintain cellular homeostasis in a process called autophagy. Autophagy involves the engulfment of cellular cargo in a structure called an autophagosome, which fuses with lysosomes resulting in cargo degradation. Whitmarsh-Everiss and Laraia discuss recent developments in identification of activators and inhibitors of distinct steps of this processes. In particular, small-molecule inhibitors that target valosin-containing protein (VCP), an ATPase that initiates autophagy, revealed a novel interaction of VCP with another autophagy protein, Beclin-1.

Despite the advances made, the major and minor moments of a cell’s lifetime remain largely hidden and are ripe for discovery. We envision that chemical biology will continue to play a central role in the development of tools and reagents to help further elucidate these hidden and known moments. We hope that the pieces in this issue will inspire and motivate more partnerships that will help drive the field forward and enable new discoveries.


Scientists create tiny RNA molecule with big implications for life's origins

An extremely small RNA molecule created by a University of Colorado at Boulder team can catalyze a key reaction needed to synthesize proteins, the building blocks of life. The findings could be a substantial step toward understanding "the very origin of Earthly life," the lead researcher contends.

The smallest RNA enzyme ever known to perform a cellular chemical reaction is described in a paper published in the Proceedings of the National Academy of Sciences. The paper was written by CU graduate student Rebecca Turk, research associate Nataliya Chumachenko and Professor Michael Yarus of the molecular, cellular and developmental biology department.

Cellular RNA can have hundreds or thousands of its basic structural units, called nucleotides. Yarus' team focused on a ribozyme -- a form of RNA that can catalyze chemical reactions -- with only five nucleotides.

Tom Blumenthal, a professor and chair of the MCDB department, noted that Tom Cech, a Nobel laureate and distinguished professor of chemistry and biochemistry at CU, and Professor Norman Pace of MCDB, independently discovered that RNA can act as an enzyme, carrying out chemical reactions. That "pioneering work" has been carried on further by Yarus, Blumenthal said.

Because proteins are complex, one vexing question is where the first proteins came from, Blumenthal said. "It now appears that the first catalytic macromolecules could have been RNA molecules, since they are somewhat simpler, were likely to exist early in the formation of the first life forms, and are capable of catalyzing chemical reactions without proteins being present," he said.

"In this paper the Yarus group has made the amazing discovery that even an extremely tiny RNA can by itself catalyze a key reaction that would be needed to synthesize proteins," Blumenthal said. "Nobody expected an RNA molecule this small and simple to be able to do such a complicated thing as that."

The finding adds weight to the "RNA World" hypothesis, which proposes that life on Earth evolved from early forms of RNA. "Mike Yarus has been one of the strongest proponents of this idea, and his lab has provided some of the strongest evidence for it over the past two decades," Blumenthal said.

Yarus noted that the RNA World hypothesis was complicated by the fact that RNA molecules are hard to make. "This work shows that RNA enzymes could have been far smaller, and therefore far easier to make under primitive conditions, than anyone has expected."

If very simple RNA molecules such as the product of the Yarus lab could have accelerated chemical reactions in Earth's primordial stew, the chances are much greater that RNA could direct and accelerate biochemical reactions under primitive conditions.

Before the advent of RNA, most biologists believe, there was a simpler world of chemical replicators that could only make more of themselves, given the raw materials of the time, Yarus said.

"If there exists that kind of mini-catalyst, a 'sister' to the one we describe, the world of the replicators would also jump a long step closer and we could really feel we were closing in on the first things on Earth that could undergo Darwinian evolution," Yarus said.

"In other words, we may have taken a substantial step toward the very origin of Earthly life," he said. "However, keep well in mind that the tiny replicator has not been found, and that its existence will be decided by experiments not yet done, perhaps not yet imagined."

"Dr. Yarus has brought an innovative approach to bear on the key question of how complex processes originated," said Michael Bender, a biologist who oversees protein synthesis grants at the National Institutes of Health's National Institute of General Medical Sciences. "By showing that a tiny segment of RNA can perform a key step of protein synthesis, this study has provided evidence that fundamental, protein-mediated cellular processes may have arisen from RNA-based mechanisms."

Yarus' work is supported by a $415,610 grant from the NIH. In 2008 he was named a fellow of the American Association for the Advancement of Science for "meritorious efforts to advance science or its applications."


1. Introduction

Despite the enormous developments in molecular biology during the past half century, the science of biology appears to have reached a conceptual impasse. Woese [1] captured both the nature and the magnitude of the problem with his comment: "Biology today is no more fully understood in principle than physics was a century or so ago. In both cases the guiding vision has (or had) reached its end, and in both, a new, deeper, more invigorating representation of reality is (or was) called for." The issue raised by Woese is a fundamental one - to understand the genesis and nature of biological organization and to address biology's holistic, rather than just its molecular nature. Kauffman [2] expressed the difficulty in somewhat different terms: ". we know many of the parts and many of the processes. But what makes a cell alive is still not clear to us. The center is still mysterious." In effect, the provocative question, "What is Life?", raised by Schrödinger over half a century ago [3], remains unresolved, a source of unending debate. Thus, despite the recent dramatic insights into the molecular character of living systems, biology of the 21 st century is continuing to struggle with the very essence of biological reality.

At the heart of biology's crisis of identity lies its problematic relationship with the two sciences that deal with inanimate matter - physics and chemistry. While the on-going debate regarding the role of reductionist thinking in biology exemplifies the difficulties at a methodological level, the problematic relationship manifests itself beyond issues of methodology and philosophy of science. Indeed, the answers to two fundamental questions, central to understanding the life issue, remain frustratingly out of reach. First, how did life emerge, and, second, how would one go about synthesizing a simple living system? Biology cannot avoid these questions because, together with the 'what is life?' question, they form the three apexes of the triangle of holistic understanding. Being able to adequately answer any one of the questions depends on being able to answer the other two. A coherent strategy for the synthesis of a living system is not possible if one does not know what life is, and one cannot know what life is if one does not understand the principles governing its emergence. Richard Feynman's aphorism (quoted in [4]) captured the issue succinctly: "What I cannot create, I do not understand". Remarkably, the laws of physics and chemistry, the two sciences that deal with material structure and reactivity, have as yet been unable to adequately bridge between the physicochemical and biological worlds.

Despite the above-mentioned difficulties we believe that the problem is resolvable, at least in principle. If the widely held view that life did emerge from inanimate matter is correct, it suggests that the integration of animate and inanimate matter within a single conceptual framework is an achievable goal. This is true regardless of our knowledge of the detailed historical path that led from inanimate to animate. The very existence of such a pathway would be proof for that. If indeed such a conversion did take place, it suggests that particular laws of physics and chemistry, whether currently known or not, must have facilitated that transformation, and therefore those laws, together with the materials on which they operated, can form the basis for understanding the relationship between these two fundamentally distinct material forms.

In this paper we wish to build on this way of thinking and to draw the outlines of a general theory of evolution, a theory that remains firmly rooted in the Darwinian landscape, but reformulated in physicochemical terms so as to encompass both biological and non-biological systems. Such a theory, first and foremost, rests on a basic assumption: that the physicochemical principles responsible for abiogenesis, the so-called chemical phase - the stage in which inanimate matter complexified into a simple living system - are fundamentally the same as those responsible for biological evolution, though for the biological phase these principles are necessarily dressed up in biological garb. Darwin would no doubt have drawn enormous satisfaction from such a proposal, one that attempts to integrate Darwinian-type thinking into the physicochemical world. However such a sweeping assumption needs to be substantiated. Accordingly our analysis is divided into two parts. In the first part we argue for the basis of that assumption, and in second part we attempt to describe key elements of that general theory, as well as the insights that derive from it, in particular with regard to the three central questions of biology, referred to above. The analysis draws heavily on data from the emergent research area termed by Günter von Kiedrowski, 'Systems Chemistry' [5, 6]. The essence of this emergent area is to fill the chemical void between chemistry and biology by seeking the chemical origins of biological organization.


Small Molecule Screening Center

The Small Molecule Screening Center enables the discovery of cutting-edge biology on Princeton's campus through the screening and innovation of small molecule compounds. Located in Frick Laboratory, the screening center collaborates with research groups in all areas of the biological sciences.

The Center’s unique compound collection and its screening capabilities make major contributions to various research activities, accelerating the identification of exceptional chemical probes in pioneering biological studies and potential therapeutic candidates of high impact.

The establishment of the screening center was made possible by the generous support from the Office of the Provost and founding contributions from the Departments of Chemistry, Molecular Biology and the Lewis-Sigler Institute for Integrative Genomics.

For more information about the research at the screening center and potential collaborations, contact Dr. Hahn Kim, Director of the Small Molecule Screening Center.


What are chemical candidates for replicator molecule? - Biology

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